Getting Pumped about Heart Failure Douglas L. Mann  Cell Metabolism  Volume 19, Issue 6, Pages 896-897 (June 2014) DOI: 10.1016/j.cmet.2014.05.008 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 Potential Model of Dysregulated Excitation-Contraction Coupling in Heart Failure Tissue injury in heart failure leads to increased expression levels of microRNA-25 (miR-25) in the heart. miR-25 binds to messenger RNA for sarcoendoplasmic reticulum Ca2+-ATPase (SERCA2a), which is responsible for pumping cytoplasmic calcium (Ca2+) into the sarcoplasmic reticulum (SR) during relaxation of the heart. Decreased expression levels of SERCA2a result in impaired uptake of cytoplasmic Ca2+ into sarcoendoplasmic reticulum, which leads to diminished pumping capacity of the heart because there is less Ca2+ available for activation of the actin and myosin crossbridges at the onset of the muscle contraction. Sustained pump dysfunction contributes to the development of the clinical syndrome of heart failure. Blocking miR-25 may represent a novel strategy for improving the pumping capacity of the heart in heart failure. Cell Metabolism 2014 19, 896-897DOI: (10.1016/j.cmet.2014.05.008) Copyright © 2014 Elsevier Inc. Terms and Conditions